Scientists say they have cracked the genetic code of breast and colon cancers, letting them "study the enemy's game plan.”
The breakthrough comes from a huge effort led by researchers at Johns Hopkins Kimmel Cancer Center. It's not the first-ever look at cancer genes. But it's the first time scientists have used 21st-century technology to scan the entire genome of breast and colon cancers, says Will Parsons, MD, PhD.
Parsons, a Johns Hopkins and National Cancer Institute researcher, is a member of the research team, which includes Victor E. Velculescu, MD, PhD; Bert Vogelstein, MD; and Kenneth W. Kinzler, PhD, of Johns Hopkins.
"We already know that cancer is the result of a series of mutations in normal cells," Parsons tells WebMD. "Now we have a blueprint for how that works."
How important is this finding?
It's not going to help people now suffering from cancer. But for researchers trying to find future cancer treatments, this is very big news. That's why Elias A. Zerhouni, MD, director of the National Institutes of Health, calls the findings "truly remarkable" and "groundbreaking."
The findings appear in the Sept. 7 online issue of Sciencexpress.
Complex Cancer Game Plan
The Johns Hopkins team painstakingly analyzed more than 13,000 genes in 11 breast cancers and 11 colon cancers.
They hoped to find that just a handful of genes cause cancer. Instead, they found some 200 cancer-related genes.
The researchers also hoped they'd find some gene mutations common to all cancers -- or at least genes common to all breast or colon cancers. That didn't happen, either. Each tumor had about a dozen cancer-related mutations that differed from tumor to tumor.
"The genetic basis of colon cancer and breast cancer are quite different; if we look at the most important genes, only two mutations occur on both lists," Parsons says. "I wasn't expecting it to be quite that diverse.
“And even if we look at two tumors of the same kind -- two colon cancers -- they would be very different. None had more than six genes mutated in common", says Parsons.
The complexity is intimidating but not totally unexpected. It simply means there won't be a magic bullet. Researchers will have to look at each kind of cancer to tease out treatment targets.
This isn't bad news -- it's biology, says Harold J. Burstein, MD, PhD, of Harvard Medical School and the Dana Farber Cancer Institute in Boston.
"If you are the Army Corps of Engineers rebuilding New Orleans, you need to know how many weak links you have in the levees," Burstein tells WebMD. "If you guess four or five, and it's 20, you have not fixed the problem. So if in cancer, you look only at four or five genes and there really are a dozen, you have a problem."
Burstein notes that the study wasn't able to say which mutations happen in which order. He says it's possible many of the mutations occur only after the tumor is growing wildly, and it may yet be possible to pinpoint a smaller number of truly significant mutations.
"The transformation from normal cells to cancer cells is still a complicated problem," Burstein says. "What we hope we have here is a roadmap to help us go after them."
Where that roadmap eventually will lead is to a new generation of targeted cancer therapies, says Parsons.
"New cancer treatments like Gleevec for leukemia, and Herceptin for breast cancer, are based on knowing the genetic basis of these cancers," Parson's says. "We will be able to come up with more of these treatments based on the huge amount of information that will become available from studies like this.”
By Daniel J. DeNoon, reviewed by Louise Chang, MD
SOURCES: Sjöblom, T. Sciencexpress, Sept. 7, 2006; online edition. Will Parsons, MD, PhD, pediatric oncology fellow, Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Md. Harold J. Burstein, MD, PhD, Harvard Medical School and Dana Farber Cancer Institute, Boston. News release, National Institutes of Health/National Human Genome Research Institute. News release, Johns Hopkins Kimmel Cancer Center.